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Biomedical subjects

A Sarabhai

Publications and source records attributed to A Sarabhai.

9 recordsLinked to original sources

Cloning of Beneckea genes in Escherichia coli.

Genes from Beneckea harveyi, a luminescent marine bacterium, were cloned in Escherichia coli. This was done by producing randomly sheared fragments of Beneckea DNA and inserting them into the EcoRI site of plasmid pMB9 by the adenine-thymine joining procedure. The hybrid plasmids were used to transform E. coli C600 SF8. Among the transformants selected for tetracycline resistance, one clone that appeared to complement a leucine tb mutation was identified. The transformants were screened for the presence of Beneckea 5S genes. Four of these clones were analyzed in detail by hybridization with 16S, 23S, and 4S Beneckea RNA. The observations suggest that the ribosomal genes in Beneckea are linked, but are present in a different order than those in E. coli.

DNA, Bacterial

Transfer RNA synthesis in vitro.

During infection of Escherichia coli, bacteriophage T4 directs the synthesis of at least eight transfer RNAs and of two stable RNA species of low molecular weight, of unknown function. When T4 DNA is incubated with purified RNA polymerase and the appropriate substrates, a high molecular weight RNA is produced. This RNA, on further incubation with a supernatant fraction prepared from E. coli, is cleaved to several species of RNA. These cleaved RNAs were analyzed by gel electrophoresis and fingerprint techniques, and were found to be similar or identical to those made in vivo. The fingerprint analysis of one of these, a tRNA(Gly), is presented. The molecule made in vitro, except for the absence of modified bases, appears to be identical to the RNA made by T4-infected cells. Therefore, in this system the tRNA genes are transcribed with fidelity, the transcript is cleaved correctly, and the tRNAs are made in good yield.

Base Sequence

Mechanism of proflavin mutagenesis.

The mutagenic action of proflavin on bacteriophage T4 is greater in the presence of defective T4 ligase than in the presence of normal T4 ligase. This suggests that the persistence of single-strand breaks in DNA enhances proflavin mutagenesis.

Coliphages